It is our objective to define the contribution of the sarcoplasmic reticulum in situ in the regulation of myoplasmic pCa and to test the applicability of our model of substrate inhibition to the regulation of tension of ATPase activity of mechanically and chemically skinned heart and skeletal muscle fibers. Solutions will be devised to independently buffer and vary the pCa, pS, ionic strength, and constituent anions and cations so as to isolate the contribution of each to controlling the tension.